Selective inhibition of platelet aggregation, without inhibition of synthesis of vasodilator prostaglandins, would maximize potential for benefit in ischemic heart disease. If possible, treatment of ischemic heart disease should utilize doses of aspirin that produce such selective inhibition. We therefore tested the relative sensitivity of platelet aggregation and prostaglandin mediated coronary vasodilatation to inhibition by aspirin. Effects of increasing doses of systemically administered aspirin on ADP-induced platelet aggregation and on arachidonic acid induced increments in coronary blood flow were determined in dogs. The dose response curves of inhibition by aspirin were similar in the two test systems. Thus we did not find selective inhibition of platelet activity at any dose of aspirin, even in the minimally effective range.